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Renal dysfunction predicts attenuation of ischemic heart disease mortality risk from elevated glucose among treated

Susan M Hailpern1, Hillel W Cohen, Michael H Alderman

  • 1Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York 10461, USA. shailper@aecom.yu.edu

American Journal of Hypertension
|October 10, 2006
PubMed

Insights

Impaired fasting glucose (IFG) increases ischemic heart disease (IHD) mortality risk in hypertensive patients with normal kidney function, but this risk is reduced in those with moderate renal dysfunction (MRD). Further research is needed.

Area of Science:

  • Cardiology
  • Nephrology
  • Endocrinology

Background:

  • Impaired fasting glucose (IFG) and renal dysfunction are independent risk factors for adverse cardiovascular outcomes.
  • Hypertension management is crucial for reducing cardiovascular events.

Purpose of the Study:

  • To investigate the interaction between renal dysfunction and IFG on the risk of ischemic heart disease (IHD) mortality.
  • To analyze this interaction in treated hypertensive subjects.

Main Methods:

  • Utilized data from 9918 participants in a worksite-based antihypertensive treatment program.
  • Employed Cox proportional hazard models to assess IHD mortality risk.
  • Stratified analysis by moderate renal dysfunction (MRD) using estimated glomerular filtration rate (GFR).

Main Results:

  • The interaction between MRD and IFG significantly improved the predictive model for IHD mortality (P = .001).
  • IFG was associated with a 47% increased IHD mortality hazard ratio in individuals with GFR ≥60 mL/min/1.73 m2.
  • Conversely, IFG was associated with a 56% decreased IHD mortality hazard ratio in individuals with MRD (GFR 30-60 mL/min/1.73 m2).

Conclusions:

  • Renal dysfunction appears to attenuate the risk of IHD mortality associated with IFG in treated hypertensive patients.
  • The observed interaction suggests a potential counter-regulatory mechanism requiring further investigation.
  • This finding highlights the complex interplay between glucose metabolism, kidney function, and cardiovascular risk.
Abstract

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